Ocular inflammation and its sequelae are a main cause of blindness in the world. Hypersensitivity is a major cause of inflammation and is thought to play a role in such blinding diseases as trachoma and phlyctenulosis. In order ultimately to have a rational basis for prevention and therapy of such complex inflammatory diseases of the eye, it is necessary first to study each type of hypersensitivity as it may occur in ocular tissues in a pure, even if mild, form. It is proposed to study ocular anaphylaxis, defined as an acute inflammatory response of the ocular tissues caused by immunologically induced release of chemical mediators. The 3 components necessary for anaphylaxis, homocytotropic antibody, mast cells or basophils, and chemical mediators, are to be studied in ocular tissues in vitro and in vivo in the Nippostrongylus brasiliensis sentized rat. The location and number of mast cells in and around the rat eye are to be determined by histologic counts. The ability of ocular tissues to participate in antigen-induced histamine release is to be assessed in an in vitro model using chopped conjunctiva from sensitized rats. An in vivo model is to be developed in which ocular tissues are passively sensitized with homocytotropic antibody. Anaphylaxis is to be assessed by increased vascular permeability as shown by leakage of Evans blue dye into ocular tissues. The requirements for passive conjunctival anaphylaxis are to be determined by selectively interrupting certain arms of the inflammatory pathways including degranulating mast cells with distilled water, producing a leukopenia with nitrogen mustard, and inactivating homocytotropic antibodies, IgE and IgGa. Characteristics of inflammatory infiltrates are to be studied histologically in acute and chronically produced anaphylaxis. The clinical, cellular, and histamine release patterns of locally produced versus systemically produced anaphylaxis of ocular structures are to be compared.